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UNITED NATIONS ENVIRONMENT PROGRAMME INTERNATIONAL LABOUR ORGANISATION WORLD HEALTH ORGANIZATION INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organisation, or the World Health Organization. Environmental Health Criteria 195 First draft prepared by Mr R. Newhook and Ms W. Dormer, Health Criteria, Canada Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization, and produced within the framework of the Inter-Organization Programme for the Sound Management of Chemicals. World Health Organization Geneva, 1997
venture of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization. The main objective of the IPCS is to carry out and disseminate evaluations of the effects of chemicals on human health and the quality of the environment. Supporting activities include the development of epidemiological, experimental laboratory, and risk-assessment methods that could produce internationally comparable results, and the development of manpower in the field of toxicology. Other activities carried out by the IPCS include the development of know-how for coping with chemical accidents, coordination of laboratory testing and epidemiological studies, and promotion of research on the mechanisms of the biological action of chemicals.
3. Environmental exposure I. Series ISBN 92 4 157195 0 (NLM Classification: QV 633) ISSN 0250-863X The World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full. Applications and enquiries should be addressed to the Office of Publications, World Health Organization, Geneva, Switzerland, which will be glad to provide the latest information on any changes made to the text, plans for new editions, and reprints and translations already available.
protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
and analytical methods 1.2. Sources of human and environmental exposure 1.3. Environmental transport, distribution and transformation 1.4. Environmental levels and human exposure 1.5. Kinetics and metabolism in laboratory animals and humans 1.6. Effects on laboratory animals and in vitro tests 1.7. Effects on humans 1.8. Effects on other organisms in the laboratory and field 1.9. Evaluation of human health risks and effects on the environment 1.9.1. Health effects 1.9.2. Environmental effects 1.10. Conclusions 2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL METHODS
2.2. Physical and chemical properties 2.3. Analytical methods 3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 3.1. Sources, uses and production processes 3.2. World production levels 3.3. Entry into the environment 4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION AND TRANSFORMATION 4.1. Environmental transport and degradation 4.2. Bioaccumulation and biomagnification 5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 5.1. Environmental levels 5.1.1. Air 5.1.2. Water 5.1.3. Soil 5.1.4. Sediment 5.1.5. Biota 5.1.6. Food and drinking-water 5.2. General population exposure 5.2.1. Human tissues and fluids 5.2.2. Intake from ambient air 5.2.3. Intake from drinking-water 5.2.4. Intake from foods 5.2.5. Apportionment of intakes 5.2.6. Trends in exposure of the general population over time 5.2.7. Occupational exposure during manufacture, formulation or use 6. KINETICS AND METABOLISM 6.1. Aquatic and terrestrial biota 6.2. Mammals 7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS 7.1. Single exposure 7.2. Short-term and subchronic exposure 7.3. Long-term toxicity and carcinogenicity 7.4. Mutagenicity and related end-points 7.5. Reproductive and developmental toxicity 7.6. Immunotoxicity 8. EFFECTS ON HUMANS 8.1. General population exposure 8.2. Occupational exposure 9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD 9.1. Short-term exposure 9.1.1. Aquatic biota 9.1.2. Terrestrial biota 9.2. Long-term exposure 9.2.1. Aquatic biota 9.2.2. Terrestrial biota 10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT 10.1. Evaluation of human health risks 10.1.1. Exposure 10.1.2. Health effects 10.1.3. Approaches to risk assessment 10.1.3.1 Non-neoplastic effects 10.1.3.2 Neoplastic effects
THE ENVIRONMENT 12. FURTHER RESEARCH 12.1. Environment 12.2. Human health 13. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES REFERENCES RÉSUMÉ ET CONCLUSIONS RÉSUMEN Y CONCLUSIONES
Every effort has been made to present information in the criteria monographs as accurately as possible without unduly delaying their publication. In the interest of all users of the Environmental Health Criteria monographs, readers are requested to communicate any errors that may have occurred to the Director of the International Programme on Chemical Safety, World Health Organization, Geneva, Switzerland, in order that they may be included in corrigenda.
International Register of Potentially Toxic Chemicals, Case postale 356, 1219 Châtelaine, Geneva, Switzerland (telephone no. + 41 22 - 9799111, fax no. + 41 22 - 7973460, E-mail irptc@unep.ch). * * * This publication was made possible by grant number 5 U01 ES02617- 15 from the National Institute of Environmental Health Sciences, National Institutes of Health, USA, and by financial support from the European Commission and the Federal Ministry for the Environment, Nature Conservation and Nuclear Safety, Germany.
initiated with the following objectives: (i) to assess information on the relationship between exposure to environmental pollutants and human health, and to provide guidelines for setting exposure limits;
pollutants; (iv) to promote the harmonization of toxicological and epidemiological methods in order to have internationally comparable results.
mercury, was published in 1976 and since that time an ever-increasing number of assessments of chemicals and of physical effects have been produced. In addition, many EHC monographs have been devoted to evaluating toxicological methodology, e.g., for genetic, neurotoxic, teratogenic and nephrotoxic effects. Other publications have been concerned with epidemiological guidelines, evaluation of short-term tests for carcinogens, biomarkers, effects on the elderly and so forth.
and the importance of environmental effects, in addition to health effects, has been increasingly emphasized in the total evaluation of chemicals. The original impetus for the Programme came from World Health Assembly resolutions and the recommendations of the 1972 UN Conference on the Human Environment. Subsequently the work became an integral part of the International Programme on Chemical Safety (IPCS), a cooperative programme of UNEP, ILO and WHO. In this manner, with the strong support of the new partners, the importance of occupational health and environmental effects was fully recognized. The EHC monographs have become widely established, used and recognized throughout the world.
Development and the subsequent establishment of the Intergovernmental Forum on Chemical Safety with the priorities for action in the six programme areas of Chapter 19, Agenda 21, all lend further weight to the need for EHC assessments of the risks of chemicals.
on the effect on human health and the environment of chemicals and of combinations of chemicals and physical and biological agents. As such, they include and review studies that are of direct relevance for the evaluation. However, they do not describe every study carried out. Worldwide data are used and are quoted from original studies, not from abstracts or reviews. Both published and unpublished reports are considered and it is incumbent on the authors to assess all the articles cited in the references. Preference is always given to published data. Unpublished data are only used when relevant published data are absent or when they are pivotal to the risk assessment. A detailed policy statement is available that describes the procedures used for unpublished proprietary data so that this information can be used in the evaluation without compromising its confidential nature (WHO (1990) Revised Guidelines for the Preparation of Environmental Health Criteria Monographs. PCS/90.69, Geneva, World Health Organization).
whenever available, are preferred to animal data. Animal and in vitro studies provide support and are used mainly to supply evidence missing from human studies. It is mandatory that research on human subjects is conducted in full accord with ethical principles, including the provisions of the Helsinki Declaration. The EHC monographs are intended to assist national and international authorities in making risk assessments and subsequent risk management decisions. They represent a thorough evaluation of risks and are not, in any sense, recommendations for regulation or standard setting. These latter are the exclusive purview of national and regional governments. Content The layout of EHC monographs for chemicals is outlined below. * Summary - a review of the salient facts and the risk evaluation of the chemical * Identity - physical and chemical properties, analytical methods * Sources of exposure * Environmental transport, distribution and transformation * Environmental levels and human exposure * Kinetics and metabolism in laboratory animals and humans * Effects on laboratory mammals and in vitro test systems * Effects on humans * Effects on other organisms in the laboratory and field * Evaluation of human health risks and effects on the environment * Conclusions and recommendations for protection of human health and the environment
* Previous evaluations by international bodies, e.g., IARC, JECFA, JMPR
meetings of scientists to establish lists of priority chemicals for subsequent evaluation. Such meetings have been held in: Ispra, Italy, 1980; Oxford, United Kingdom, 1984; Berlin, Germany, 1987; and North Carolina, USA, 1995. The selection of chemicals has been based on the following criteria: the existence of scientific evidence that the substance presents a hazard to human health and/or the environment; the possible use, persistence, accumulation or degradation of the substance shows that there may be significant human or environmental exposure; the size and nature of populations at risk (both human and other species) and risks for environment; international concern, i.e. the substance is of major interest to several countries; adequate data on the hazards are available.
priority list, the IPCS Secretariat consults with the Cooperating Organizations and all the Participating Institutions before embarking on the preparation of the monograph. Procedures The order of procedures that result in the publication of an EHC monograph is shown in the flow chart. A designated staff member of IPCS, responsible for the scientific quality of the document, serves as Responsible Officer (RO). The IPCS Editor is responsible for layout and language. The first draft, prepared by consultants or, more usually, staff from an IPCS Participating Institution, is based initially on data provided from the International Register of Potentially Toxic Chemicals, and reference data bases such as Medline and Toxline.
initial review by a small panel of experts to determine its scientific quality and objectivity. Once the RO finds the document acceptable as a first draft, it is distributed, in its unedited form, to well over 150 EHC contact points throughout the world who are asked to comment on its completeness and accuracy and, where necessary, provide additional material. The contact points, usually designated by governments, may be Participating Institutions, IPCS Focal Points, or individual scientists known for their particular expertise. Generally some four months are allowed before the comments are considered by the RO and author(s). A second draft incorporating comments received and approved by the Director, IPCS, is then distributed to Task Group members, who carry out the peer review, at least six weeks before their meeting. The Task Group members serve as individual scientists, not as representatives of any organization, government or industry. Their function is to evaluate the accuracy, significance and relevance of the information in the document and to assess the health and environmental risks from exposure to the chemical. A summary and recommendations for further research and improved safety aspects are also required. The composition of the Task Group is dictated by the range of expertise required for the subject of the meeting and by the need for a balanced geographical distribution.
important role played by nongovernmental organizations. Representatives from relevant national and international associations may be invited to join the Task Group as observers. While observers may provide a valuable contribution to the process, they can only speak at the invitation of the Chairperson. Observers do not participate in the final evaluation of the chemical; this is the sole responsibility of the Task Group members. When the Task Group considers it to be appropriate, it may meet in camera.
participate in the preparation of the EHC monograph must, in addition to serving in their personal capacity as scientists, inform the RO if at any time a conflict of interest, whether actual or potential, could be perceived in their work. They are required to sign a conflict of interest statement. Such a procedure ensures the transparency and probity of the process.
satisfied as to the scientific correctness and completeness of the document, it then goes for language editing, reference checking, and preparation of camera-ready copy. After approval by the Director, IPCS, the monograph is submitted to the WHO Office of Publications for printing. At this time a copy of the final draft is sent to the Chairperson and Rapporteur of the Task Group to check for any errors.
updating of an EHC monograph: new data are available that would substantially change the evaluation; there is public concern for health or environmental effects of the agent because of greater exposure; an appreciable time period has elapsed since the last evaluation. All Participating Institutions are informed, through the EHC progress report, of the authors and institutions proposed for the drafting of the documents. A comprehensive file of all comments received on drafts of each EHC monograph is maintained and is available on request. The Chairpersons of Task Groups are briefed before each meeting on their role and responsibility in ensuring that these rules are followed.
Hacettepe University, Hacettepe, Ankara, Turkey Professor B. Jansson, Institute of Applied Environmental Research, ITM-Solna, Stockholm University, Stockholm, Sweden Dr J. Jarrell, Foothills Hospital, Calgary Regional Health Authority, Calgary, Alberta, Canada Dr A. Langley, South Australian Health Commission, Rundle Mall, Australia ( Chairman) Mr R. Newhook, Bureau of Chemical Hazards, Environmental Substances Division, Health Canada, Tunney's Pasture, Ottawa, Ontario, Canada ( Rapporteur)
( Vice-chairman) Dr A.G. Smith, Medical Research Council Toxicology Unit, Hodgkin Building, University of Leicester, Leicester, United Kingdom
Institut Municipal d'Investigacio Medica, Barcelona, Spain Dr A. van Birgelen, National Health and Environmental Effects Research Laboratory, Pharmacokinetics Branch, US Environmental Protection Agency, Research Triangle Park, North Carolina, USAa
(RIVM), Hygiene, Bilthoven, The Netherlands a Dr A. Van Birgelen's present address: National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
Toxicology, Brussels, Belgium (Representing EURO CHLOR) Dr Roger Drew, Toxicology Information Section, Safety, Health & Environment Division, ICI Australia Operations Pty Ltd., ICI House, Melbourne, Victoria, Australia (Representing European Centre for Ecotoxicology and Toxicology of Chemicals) Secretariat Dr G.C. Becking, Interregional Research Unit, International Programme on Chemical Safety, Research Triangle Park, North Carolina USA ( Secretary)
Substances Division, Health Canada, Tunney's Pasture, Ottawa, Ontario, Canada ( Temporary Adviser to Secretariat)
International Agency for Research on Cancer, Lyon, France IPCS TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR HEXACHLOROBENZENE A WHO Task Group on Environmental Health Criteria for Hexachlorobenzene met in Geneva from 26 February to 1 March 1996. Dr G.C. Becking, IPCS, welcomed the participants on behalf of Dr M. Mercier, Director of the IPCS, and the three cooperating organizations (UNEP/ILO/WHO). The group reviewed and revised the draft and made an evaluation of the risks for human health and the environment from exposure to hexachlorobenzene.
Health Canada, Ottawa, Canada. These authors also prepared the draft reviewed by the Task Group, which incorporated the comments received following circulation of the first draft to IPCS Contact Points for Environmental Health Criteria monographs.
of the Health Protection Branch, Health Canada. This support was indispensable for the completion of this monograph.
Unit) and Dr P.G. Jenkins (IPCS, Central Unit, Geneva) were responsible for the overall scientific content and the technical editing, respectively, of this monograph. The efforts of all who helped in the preparation and finalization of this publication are gratefully acknowledged. ABBREVIATIONS BCF bioconcentration factor BMF biomagnification factor DL detection limit HCB hexachlorobenzene i.p. intraperitoneal ND not detectable PCT porphyria cutanea tarda p,p'DDE 1,1'-(2,2-dichloroethylidene)-bis[4-chlorobenzene] SER smooth endoplasmic reticulum T3 triiodothyronine T4 thyroxine
(EHC), as outlined in the Preamble of this monograph, is an extremely time-consuming and resource-intensive procedure. Often countries have prepared recent comprehensive reviews on chemicals as required by their national legislation, and the International Programme on Chemical Safety (IPCS) has been asked by Member States to determine how best to utilize such national reviews during the preparation of international EHC. Utilizing such national documents should avoid duplication of effort and result in the more rapid production of more concise IPCS EHC monographs. This monograph on hexachlorobenzene has been prepared using as background document the review (Supporting Document) prepared under the Canadian Environmental Protection Act (CEPA), dated June 1993. From this document, staff of Health Canada have chosen only the most relevant studies for assessing the human and environmental risks from exposure to hexachlorobenzene. These have been described from the original references and supplemented by additional information published more recently. This has resulted in a concise monograph, yet one that supplies sufficient information for the reader to understand the basis for the conclusions reached by the Task Group. Readers who wish to consult the text of the Canadian Supporting Document can obtain a copy from the Director, IPCS, World Health Organization, Geneva, Switzerland.
analytical methods Hexachlorobenzene (HCB) is a chlorinated organic compound with moderate volatility. It is practically insoluble in water, but is highly lipid-soluble and bioaccumulative. Technical grade HCB contains up to 2% impurities, most of which is pentachlorobenzene. The remainder includes the higher chlorinated dibenzo- p-dioxins, dibenzofurans and biphenyls. Analysis of HCB in environmental media and biological materials generally involves extraction of the sample into organic solvents, often followed by a clean-up step, to produce organic extracts for gas chromatography/mass spectrometry (GC/MS) or gas chromatography with electron capture detection (GC/ECD). 1.2 Sources of human and environmental exposure HCB was at one time used extensively as a seed dressing to prevent fungal disease on grains, but this use was discontinued in most countries in the 1970s. HCB continues to be released to the environment from a number of sources, including the use of some chlorinated pesticides, incomplete combustion, old dump sites and inappropriate manufacture and disposal of wastes from the manufacture of chlorinated solvents, chlorinated aromatics and chlorinated pesticides. 1.3 Environmental transport, distribution and transformation HCB is distributed throughout the environment because it is mobile and persistent, although slow photodegradation in air and microbial degradation in soil do occur. In the troposphere, HCB is transported long distances and removed from the air phase through deposition to soil and water. Significant biomagnification of HCB through the food chain has been reported. 1.4 Environmental levels and human exposure Low concentrations of HCB are present in ambient air (a few ng/m3 or less) and in drinking-water and surface water (a few ng/litre or less) in areas that are distant from point sources around the world. However, higher levels have been measured near point sources. HCB is bioaccumulative and has been detected in invertebrates, fish, reptiles, birds and mammals (including humans) distant from point sources, particularly in fatty tissues of organisms at higher trophic levels. Mean levels in adipose tissue of the human general population in various countries range from tens to hundreds of ng/g wet weight. Based on representative levels of HCB in air, water and food, the total intake of HCB by adults in the general population is estimated to be between 0.0004 and 0.003 µg/kg body weight per day. This intake is predominantly from the diet. Owing to the presence of HCB in breast milk, mean intakes by nursing infants have been estimated to range from < 0.018 to 5.1 µg/kg body weight per day in various countries. The results of most studies on the levels of HCB in foods and human tissues over time indicate that exposure of the general population to HCB declined from the 1970s to the mid-1990s in many locations. However, this trend has not been evident during the last decade in some other locations. 1.5 Kinetics and metabolism in laboratory animals and humans There is a lack of toxicokinetic information for humans. HCB is readily absorbed by the oral route in experimental animals and poorly via the skin (there are no data concerning inhalation). In animals and humans, HCB accumulates in lipid-rich tissues, such as adipose tissue, adrenal cortex, bone marrow, skin and some endocrine tissues, and can be transferred to offspring both across the placenta and via mothers' milk. HCB undergoes limited metabolism, yielding pentachlorophenol, tetrachlorohydroquinone and pentachlorothiophenol as the major metabolites in urine. Elimination half-lives for HCB range from approximately one month in rats and rabbits to 2 or 3 years in monkeys.
The acute toxicity of HCB to experimental animals is low (1000 to 10 000 mg/kg body weight). In animal studies, HCB is not a skin or eye irritant and does not sensitize the guinea-pig.
the pathway for the biosynthesis of haem is a major target of hexachlorobenzene toxicity. Elevated levels of porphyrins and/or porphyrin precursors have been found in the liver, other tissues and excreta of several species of laboratory mammals exposed to HCB. Porphyria has been reported in a number of studies in rats with subchronic or chronic oral exposure to between 2.5 and 15 mg HCB/kg body weight per day. Excretion of coproporphyrins was increased in pigs ingesting 0.5 mg HCB/kg body weight per day or more (no effects were observed at 0.05 mg HCB/kg body weight per day in the latter study). Repeated exposure to HCB has also been shown to affect a wide range of organ systems (including the liver, lungs, kidneys, thyroid, skin, and nervous and immune systems), although these have been reported less frequently than porphyria. HCB is a mixed-type cytochrome-P-450-inducing compound, with phenobarbital-inducible and 3-methylcholanthrene-inducible properties. It is known to bind to the Ah receptor.
changes, enzyme induction) occurred in several studies of rats exposed to between 0.25 and 0.6 mg HCB/kg body weight per day; the NOELs in these studies were 0.05 to 0.07 mg HCB/kg body weight per day. Concentrations of neurotransmitters in the hypothalamus were altered in mink dams with chronic dietary exposure to 0.16 mg HCB/kg body weight per day, and in their offspring exposed throughout gestation
in subchronic studies on rats at 0.7 mg HCB/kg body weight per day, but not at 0.07 mg/kg body weight per day.
bioassays on rodents. In hamsters fed diets yielding average doses of 4, 8 or 16 mg/kg body weight per day for life, there were increases in the incidence of liver cell tumours (hepatomas) in both sexes at all doses, haemangioendotheliomas of the liver at 8-16 mg/kg body weight per day, and adenomas of the thyroid in males at the highest dose. Dietary exposure of mice to 6, 12 and 24 mg/kg body weight per day for 120 weeks resulted in an increase in the incidence of liver cell tumours (hepatomas) in both sexes at the two higher doses (not significant, except for females at the highest dose). In utero, lactational and oral exposure of rats to HCB in diets yielding average lifetime doses ranging from 0.01 to 1.5 mg/kg body weight per day (males) or 1.9 mg/kg body weight per day (females) for up to 130 weeks
neoplastic liver nodules and adrenal phaeochromocytomas in females and of parathyroid adenomas in males. In another long-term study on rats, exposure for up to 2 years to diets yielding average HCB doses of 4-5 and 8-9 mg/kg body weight per day induced increases in the incidences of hepatomas and of renal cell adenomas at both doses in both sexes, and of hepatocellular carcinomas, bile duct adenomas/ carcinomas and adrenal phaeochromocytomas and adrenal cortical adenomas in females. High incidences of liver tumours have also been reported in some more limited studies in which single dietary concentrations were administered to small groups of female rats. In addition, it has been reported that, following subchronic dietary exposure to HCB, mice, hamsters and rats developed tumours in the liver, bile duct, kidney, thymus, spleen and lymph nodes. Dietary exposure to HCB promoted the induction of liver tumours by polychlorinated terphenyl in mice and by diethylnitrosamine in rats. Except in the case of renal tumours in male rats (which appear at least in part to be the result of hyaline droplet nephropathy) and hepatomas in rats (which may result from hyperplastic responses to hepatocellular necrosis), mechanistic studies that address the relevance to humans of the tumour types induced by HCB have not been identified. HCB has little capability to induce directly gene mutation, chromosomal damage and DNA repair. It exhibited weak mutagenic activity in a small number of the available studies on bacteria and yeast, although it should be noted that each of these studies has limitations. There is also some evidence of low-level binding to DNA
genotoxic carcinogens. In studies of reproduction, oral exposure of monkeys to as little as 0.1 mg HCB/kg body weight per day for 90 days affected the light microscopic structure and ultrastructure of the surface germinal
caused ultrastructural injury to the primordial germ cells. These specific target sites, which are damaged further at higher doses, were associated with otherwise normal follicular, oocyte and embryo development, suggesting specificity of HCB action within the site of the ovary. Male reproduction was only affected at much higher doses (between 30 and 221 mg/kg body weight per day) in studies on several non-primate species. Transplacental or lactational exposure of rats and cats to maternal doses of between 3 and 4 mg/kg body weight per day was found to be hepatotoxic and/or affected the survival or growth of nursing offspring. In some cases, these or higher doses reduced litter sizes and/or increased the number of stillbirths. (Adverse effects on suckling infants have generally been observed more frequently, and at lower doses, than embryotoxic or fetotoxic effects). The offspring of mink with chronic exposure to as little as 1 mg HCB/kg diet (approximately 0.16 mg/kg body weight per day) had reduced birth weight and increased mortality to weaning. Although skeletal and renal abnormalities have been observed in fetuses in some studies of rats and mice exposed to HCB during gestation, these were either not clearly related to treatment or occurred at doses that were also maternally toxic. In two studies, one of which included lactational and postnatal exposure, neurobehavioural development of rat pups was affected by in utero exposure to HCB at oral maternal doses of 0.64 to 2.5 mg HCB/kg body weight per day.
affects the immune system. Rats or monkeys exposed to between 3 and 120 mg HCB/kg body weight per day had histopathological alterations in the thymus, spleen, lymph nodes and/or lymphoid tissues of the lung. Chronic exposure of beagle dogs to 0.12 mg/kg body weight per day caused nodular hyperplasia of the gastric lymphoid tissue. In a number of studies on rats, humoral immunity and, to a lesser extent, cell- mediated immunity were enhanced by several weeks exposure to HCB in the diet, while macrophage function was unaltered. As little as 4 mg HCB/kg diet (approximately 0.2 mg/kg body weight per day) during gestation, through nursing and to 5 weeks of age increased humoral and cell-mediated immune responses and caused accumulation of macrophages in the lung tissue of rat pups. In contrast, HCB has been found to be immunosuppressive in most studies with mice; doses of as little as 0.5-0.6 mg/kg body weight per day for several weeks depressed resistance to infection by Leishmania or to a challenge with tumour cells, decreased cytotoxic macrophage activity of the spleen, and reduced the delayed-type hypersensitivity response in offspring exposed in utero and through nursing. In a number of studies on various strains of rats, short-term or subchronic exposure to HCB affected thyroid function, as indicated by decreased serum levels of total and free thyroxine (T4) and often, to a lesser extent, triiodothyronine (T3).
accidental poisonings that took place in Turkey in 1955-1959, in which more than 600 cases of porphyria cutanea tarda (PCT) were identified. In this incident, disturbances in porphyrin metabolism, dermatological lesions, hyperpigmentation, hypertrichosis, enlarged liver, enlargement of the thyroid gland and lymph nodes, and (in roughly half the cases) osteoporosis or arthritis were observed, primarily in children. Breast-fed infants of mothers exposed to HCB in this incident developed a disorder called pembe yara (pink sore), and most died within a year. There is also limited evidence that PCT occurs in humans with relatively high exposure to HCB in the workplace or in the general environment. The few available epidemiological studies of cancer are limited by small size, poorly characterized exposures to HCB and exposure to numerous other agents, and are insufficient to assess the carcinogenicity of HCB to humans. 1.8 Effects on other organisms in the laboratory and field In studies of the acute toxicity of HCB to aquatic organisms, exposure to concentrations in the range of 1 to 17 µg/litre reduced production of chlorophyll in algae and reproduction in ciliate protozoa, and caused mortality in pink shrimp and grass shrimp, but did not cause mortality in freshwater or marine fish. In longer-term studies, the growth of sensitive freshwater algae and protozoa was affected by a concentration of 1 µg/litre, while concentrations of approximately 3 µg/litre caused mortality in amphipods and liver necrosis in large-mouth bass.
to develop guidance values for non-neoplastic and neoplastic effects of HCB.
(0.05 mg HCB/kg body weight per day), for primarily hepatic effects observed at higher doses in studies on pigs and rats exposed by the oral route, and incorporating an uncertainty factor of 300 (× 10 for interspecies variation, × 10 for intraspecies variation, and × 3 for severity of effect), a TDI of 0.17 µg/kg body weight per day has been derived.
dose TD5 i.e., the intake associated with a 5% excess incidence of tumours in experimental studies in animals. Based on the results of the two-generation carcinogenicity bioassay in rats and using the multi-stage model, the TD5 value is 0.81 mg/kg body weight per day for neoplastic nodules of the liver in females. Based on consideration of the insufficient mechanistic data, an uncertainty factor of 5000 was used to develop a health-based guidance value of 0.16 µg/kg body weight per day.
studies on which an environmental risk assessment can be made. Levels of HCB in surface water are generally several orders lower than those expected to present a hazard to aquatic organisms, except in a few extremely contaminated locations. However, HCB concentrations in the eggs of sea birds and raptors from a number of locations from around the world approach those associated with reduced embryo weights in herring gulls (1500 µg/kg), suggesting that HCB has the potential to harm embryos of sensitive bird species. Similarly, levels of HCB in fish at a number of sites worldwide are within an order of magnitude of the dietary level of 1000 µg/kg associated with reduced birth weight and increased mortality of offspring in mink. This suggests that HCB has the potential to cause adverse effects in mink and perhaps other fish-eating mammals. 1.10 Conclusions a) HCB is a persistent chemical that bioaccumulates owing to its lipid solubility and resistance to breakdown. b) Animal studies have shown that HCB causes cancer and affects a wide range of organ systems including the liver, lungs, kidneys, thyroid, reproductive tissues and nervous and immune systems.
and adults, and mortality in nursing infants, has been observed in humans with high accidental exposure.
of HCB.
intake (TDI) of HCB in humans have been suggested: for non-cancer effects, 0.17 µg/kg body weight/day; for neoplastic effects, 0.16 µg/kg body weight/day.
with the chemical formula C6Cl6. Its CAS registry number is 118-74-1. 
Synonyms: perchlorobenzene, pentachlorophenyl chloride, phenyl perchloryl Trade names: Amatin, Anticarie, Bunt Cure, Bunt-No-More, Co-op Hexa, Granox NM, Julin's Carbon Chloride, No Bunt, No Bunt 40, No Bunt 80, No Bunt Liquid, Sanocide, Smut-Go, Snieciotox, HexaCB 2.2 Physical and chemical properties Some physical and chemical properties of HCB are listed in Table 1. At ambient temperature, HCB is a white crystalline that is virtually insoluble in water, but is soluble in ether, benzene and chloroform (NTP, 1994). It has a high octanol/water partition coefficient, low vapour pressure, moderate Henry's Law constant and low flammability. Technical grade HCB is available as a wettable powder, liquid and dust (NTP, 1994). Technical grade HCB contains about 98% HCB, 1.8% pentachlorobenzene and 0.2% 1,2,4,5- tetrachlorobenzene (IARC, 1979), and it is known to contain a variety of impurities, including hepta- and octachlorodibenzofurans, octachlorodibenzo- p-dioxin and decachlorobiphenyl (Villanueva et al., 1974; Goldstein et al., 1978). Table 1. Physical and chemical properties of hexachlorobenzenea Property Value Relative molecular mass 284.79 Melting point (°C) 230 Boiling point (°C) 322 (sublimates) Density (g/cm3 at 20°C 1.5691 Vapour pressure 0.0023 (Pa at 25°C) Log octanol/water partition coefficient 5.5 Water solubility 0.005 (mg/litre at 25°C) Henry's Law Constant (caluclated)b 131 (Pa/mol per m3) Conversion factors 1 ppm = 11.8 mg/m3 1 mg/m3 = 0.08 ppm a From ATSDR (1990); Mackay et al. (1992) b The Henry's Law Constant has been calculated using the tabled values for aqueous solubility and vapour pressure 2.3 Analytical methods Analytical methods for the determination of HCB in environmental samples and biological tissues vary depending upon the matrix and representative methods for various matrices, and are summarized in Tables 2 and 3. Table 2. Analytical methods for determining hexachlorobenzene in environmental samplesa Sample Sample preparation Analytical Sample Recovery Reference matrix methodb detection limit
exchange to hexane, concentrate; Florisil column chromatography as a clean-up Water Extract with dichloromethane GC/MS 1.9 mg/kg No data US EPA (1982) at pH 11 and 2, concentrate Air Glass fibre filter and XAD2 HRGC/ 0.18 pg/m3 >99% Hippelein et al. (1993) traps separated by a PUF LRMS disk; extraction with toluene
sampling cartridge, extraction with diethyl ether in hexane
plugs, extraction with hexane, range (not fractionation by HPLC specified)
(PUF), or Tenax-GC resin; effective Bidleman (1980) filters refluxed with than PUF in dichloromethane and retaining HCB chlorinated solvents removed and refluxed with hexane; clean-up by alumina chromatography Table 2 contd. Sample Sample preparation Analytical Sample Recovery Reference matrix methodb detection limit
resin separated by a silanized 95 ± 12% Nestrick (1979) glass wool plug, desorption with carbon tetrachloride. Air Trace Atmospheric Gas Analyser approx No data Thomson et al. (1980) using negative atmospheric 0.35 µg/m3 pressure chemical ionization for trace gas analysis; collection from ambient air and transfer into a carrier of CO2 for analysis
chemical 96.5±3.6% waste disposal
site samples Soil Extract with dichloromethane GC/MS 18 mg/kg No data US EPA (1986b) 5 mg/kg
to acid-base fractionation; (1983) base/neutral fraction subjected to silica gel chromatography
matrix methodb detection limit
non-water 50 mg/kg miscible
HRGC = high-resolution gas chromatography; LRMS = low-resolution mass spectrometry c Identification limit; detection limits for actual samples are several orders of magnitude higher depending upon the sample matrix and extraction procedure employed. Table 3. Analytical methods for determining hexachlorobenzene in biological materials Sample Sample preparation Analytical Sample Recovery Reference matrix method detection limit
with hexane/acetone, clean-up by 0.05 µg/kg Na2SO4/Alumina/silica gel/Florisil column followed by a H2SO4 column on silica gel
solvent and sulfuric acid partitioning
column chromatography, methylation, alumina column chromatography
tissue partitioning into petroleum ether, silica gel chromatography
tissue to Florisil clean-up and one-fraction (chicken) elution
tissue bulk lipid removal, Florisil fractionation
tissue Florisil fractionation Table 3 contd. Sample Sample preparation Analytical Sample Recovery Reference matrix method detection limit
silica gel column chromatography, (urine) Nestrick (1979) concentrate 16 µg/kg (blood)
Blood Extraction with hexane/isopropanol GC/ECD No data No data Lunde & Bjorseth (1977) Breast milk Extraction with acetone/benzene, GC/ECD 33 µg/kg 70-82% Mes et al. (1993) Florisil fractionation GC = gas chromatography; ECD = electron capture detector; PID = photoionization detector; HRGC = high-resolution gas chromatography; MS = mass spectrometry 3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 3.1 Sources, uses and production processes Industrial synthesis of HCB may be achieved through the chlorination of benzene at 150-200°C using a ferric chloride catalyst or from the distillation of residues from the production of tetrachloroethylene (US EPA, 1985a). HCB may also be synthesized by refluxing hexachlorocyclohexane isomers with sulfuryl chloride or chlorosulfonic acid in the presence of a ferric chloride or aluminum catalyst (Brooks & Hunt, 1984).
major agricultural application for HCB used to be as a seed dressing for crops such as wheat, barley, oats and rye to prevent growth of fungi. The use of HCB in such applications was discontinued in many countries in the 1970s owing to concerns about adverse effects on the environment and human health. HCB may continue to be used for this purpose in some countries; for example, HCB was still used in 1986 as a fungicide, seed-dressing and scabicide in sheep in Tunisia (Jemaa et al., 1986). However, it is uncertain as to whether HCB is still used for this purpose. In industry, HCB has been used directly in the manufacture of pyrotechnics, tracer bullets and as a fluxing agent in the manufacture of aluminum. HCB has also been used as a wood-preserving agent, a porosity-control agent in the manufacture of graphite anodes, and as a peptizing agent in the production of nitroso and styrene rubber for tyres (Mumma & Lawless, 1975). It is likely that some of these applications have been discontinued, although no information is available. Although HCB production has ceased in most countries, it is still being generated inadvertently as a by-product and/or impurity in several chemical processes. HCB is formed as a reaction by-product of thermal chlorination, oxychlorination, and pyrolysis operations in the manufacture of chlorinated solvents (mainly carbon tetrachloride, trichloroethylene and tetrachloroethylene) (Government of Canada, 1993). The concentrations of HCB in distillation bottoms was estimated to be 25%, 15% and 5%, respectively, for tetrachloroethylene, carbon tetrachloride and trichloroethylene (Jacoff et al., 1986). While HCB could potentially also be a contaminant in the final product, it was not detected (detection limit 5 mg/litre) in carbon tetrachloride and tetrachloroethylene in an investigation in Canada (personal communication to Health Canada by Mr John Schultiess, Dow Chemical Canada Inc., 1991). Analysis of production lots of tri- and tetrachloroethylene produced in Europe in 1996 failed to detect HCB at a detection limit of 2 µg/litre solvent (personal communication to the IPCS by Mr C. de Rooij, Solvay Corporation Europe, 1996).
manufacture of chlorinated solvents, chlorinated aromatics and pesticides (Jacoff et al., 1986). The waste streams from the production of pentachloronitrobenzene (PCNB), chlorothalonil and dacthal are expected to contribute the bulk of HCB released from the pesticide industry (Brooks & Hunt, 1984), although HCB can also be generated as a waste by-product from the production of pentachlorophenol, atrazine, simazine, propazine and maleic hydrazide (Quinlivan et al., 1975; Mumma & Lawless, 1975). These pesticides are also known to contain HCB as an impurity in the final product, usually at levels of less than 1% HCB when appropriate procedures are used for the synthesis and purification stages (Tobin, 1986). When such procedures are not met, the level of HCB could be much higher (e.g., pentachloronitrobenzene has been reported to contain 1.8-11% HCB (Tobin, 1986)). However, owing to many voluntary and regulatory pressures, it is unlikely that such high levels of HCB are present in today's pesticide formulations, but no information is available to substantiate this point. The chlor-alkali industry produces chlorine (Cl2), hydrogen and caustic soda (NaOH) by electrolysis of purified and concentrated sodium chloride (NaCl). Processes using graphite anodes are known to produce HCB as a by-product (Quinlivan et al., 1975; Mumma & Lawless, 1975; Alves & Chevalier, 1980) owing to the reaction of chlorine with graphite anode materials such as carbon and oils. Depending on the purification procedures, the final products might also be contaminated with HCB. In some countries, graphite anodes have been replaced by dimensionally stabilized anodes (DSA), which do not generate HCB (Government of Canada, 1993). Incineration is an important source of HCB in the environment. Emission levels from incinerators are very site-specific, and therefore generic levels are difficult to estimate. Earlier information yielded a crude estimate of the total HCB released from all municipal incinerators in the USA to be 57-454 kg/year (US EPA, 1986a), but levels currently emitted are not known. 3.2 World production levels Few recent data on the quantities of HCB produced are available. Worldwide production of pure HCB was estimated to be 10 000 tonnes/year for the years 1978-1981 (Rippen & Frank, 1986). An estimated 300 tonnes was produced by three manufacturers in the USA in 1973 (IARC, 1979). HCB was produced/imported in the European Community at 8000 tonnes/year in 1978 (Rippen & Frank, 1986), and a company in Spain used to produce an estimated 150 tonnes of HCB annually (IARC, 1979). Approximately 1500 tonnes of HCB were manufactured annually in Germany for the production of the rubber auxiliary PCTP (BUA, 1994), but this production was discontinued in 1993. No further centres of HCB manufacture in Europe or North America have been identified. Production of HCB has declined as a result of restrictions on its use starting in the 1970s.
product in the manufacture of chlorinated solvents, chlorinated aromatics and chlorinated pesticides. Jacoff et al. (1986) estimated that approximately 4130 tonnes of HCB are generated annually as a waste product in the USA and that nearly 77% of this is produced from the manufacture of three chlorinated solvents: carbon tetrachloride, trichloroethylene and tetrachloroethylene. The remainder is produced by the chlorinated pesticide industry. In 1977, about 300 tonnes of HCB were generated in Japan as a waste by-product in the production of tetrachloroethylene, almost all of which was incinerated (IARC, 1979). It was estimated that >5000 tonnes HCB/year were produced as a by- product during tetrachloroethylene production in the Federal Republic of Germany in 1980 (Rippen & Frank, 1986). However, recent estimates for Europe from ECSA (European Chlorinated Solvent Association; P.G. Johnson (1996) personal communication to IPCS) indicate that up to 4000 tonnes/year of HCB are produced as a by-product during certain tetrachloroethylene production processes and that over 99% of this by- product was incinerated at high temperatures. 3.3 Entry into the environment Currently, the principal sources of HCB in the environment are estimated to be the manufacture of chlorinated solvents, the manufacture and application of HCB-contaminated pesticides, and inadequate incineration of chlorine-containing wastes. It should be noted that only a small fraction of the HCB generated as a by-product may be released, depending on the process technology and waste- disposal practices employed. For example, according to the US Toxic Chemical Release Inventory (TRI), releases of HCB from the ten largest processing facilities were 460 kg, most of this to air, compared with almost 542 000 kg transferred offsite as waste. The TRI data are not comprehensive, since only certain types of facilities are required to report (ATSDR, 1994). ECSA (P.G. Johnson, personal communication to IPCS) estimated that European emissions of HCB were about 200 kg/year in 1993.
number of chlorinated pesticides. Since most current applications for these products are dispersive, most HCB from this source will be released to the environment.
generated through the manufacture of chlorinated solvents and pesticides. In the mid-1980s in the USA, 81% of these HCB-containing wastes were disposed of by incineration, compared to 19% via landfilling (Jacoff et al., 1986). It is likely that the amount of HCB wastes disposed of by incineration has since increased, although information has not been found to confirm this point. HCB can be emitted from incinerators as a result of incomplete thermal decomposition of these wastes and as a product of incomplete combustion (PIC) from the thermal decomposition of a variety of chlorinated organics such as Kepone, mirex, chlorobenzenes,
mixtures of chlorinated solvents (Ahling et al., 1978; Dellinger et al., 1991).
generated in the USA is landfilled, HCB may continue to leach to groundwater from previously landfilled HCB waste sites. The contribution of this route is uncertain, although HCB is not easily leached, and landfills containing HCB are now designed to prevent leachate losses into adjacent water systems (Brooks & Hunt, 1984). HCB emission into the atmosphere from landfills containing HCB wastes occurs from slow volatilization and from displacement of the contaminated soil (Brooks & Hunt, 1984).
including paint manufacturers, coal and steel producers, pulp and paper mills, textile mills, pyrotechnics producers, aluminum smelters, soap producers and wood-preservation facilities (Quinlivan et al., 1975; Gilbertson, 1979; Alves & Chevalier, 1980), probably reflecting the use of products contaminated with HCB. Municipal and industrial wastewater facilities may also discharge HCB-contaminated effluents (Environment Canada/Ontario Ministry of the Environment, 1986; King & Sherbin, 1986), probably owing to inputs from industrial sources.
redistribution of HCB throughout the environment. Wet deposition (deposition via rain or snowfall) is the primary mechanism for transport of HCB from the atmosphere to aquatic and terrestrial systems in Canada (Eisenreich & Strachan, 1992). For example, it is estimated that long-range transport and total deposition to the Canadian environment is approximately 510 kg/year, an amount that is similar to that from all other sources combined (Government of Canada, 1993).
mobile and resistant to degradation. Volatilization from water to air and sedimentation following adsorption to suspended particulates are the major removal processes from water (Oliver, 1984a; Oliver & Charlton, 1984). Once in the sediments, HCB will tend to accumulate and become trapped by overlying sediments (Oliver & Nicol, 1982). Although HCB is not readily leached from soils and sediments, some desorption does occur and may be a continuous source of HCB to the environment, even if inputs to the system cease (Oliver, 1984a; Oliver et al., 1989). Chemical or biological degradation is not considered to be important for the removal of HCB from water or sediments (Callahan et al., 1979; Mansour et al., 1986; Mill & Haag, 1986; Oliver & Carey, 1986). In the troposphere, HCB is transported over long distances by virtue of its persistence, but does undergo slow photolytic degradation (the half-life is approximately 80 days; Mill & Haag, 1986), or is removed from the air phase via atmospheric deposition to water and soil (Bidleman et al., 1986; Ballschmiter & Wittlinger, 1991; Lane et al., 1992a, 1992b). In soil, volatilization is the major removal process at the surface (Kilzer et al., 1979; Griffin & Chou, 1981; Schwarzenbach et al., 1983; Nash & Gish, 1989), while slow aerobic (half-life of 2.7-5.7 years) and anaerobic biodegradation (half-life of 10.6-22.9 years) are the major removal processes at lower depths (Beck & Hansen, 1974; Howard et al., 1991).
of its physicochemical properties (high octanol/water partition coefficient) and its slow elimination due to limited metabolism related to its high chemical stability. Organisms generally accumulate HCB from water and from food, although benthic organisms may also accumulate HCB directly from sediment (Oliver, 1984b; Knezovich & Harrison, 1988; Gobas et al., 1989). The uptake of HCB in benthic invertebrates has been investigated in a number of laboratory and field studies. The results demonstrated that some HCB in sediments is available to infaunal species. Reported bioaccumulation factorsa (BAF) for invertebrates in HCB-containing sediments range from 0.04 to 0.58 in high-organic-content sediment to 1.95 in low-organic-content a Defined as tissue concentration (wet weight) divided by sediment concentration (dry weight). BAFs from Oliver (1984b) were divided by 6.67 to convert tissue dry weight to wet weight.
1989). The bioavailability of sediment-bound HCB is inversely related to sediment organic carbon content (Knezovich & Harrison, 1988), and varies with the type and size of the organisms and their feeding habits (Boese et al., 1990), the extent of contact with sediment pore and interstitial waters (Landrum, 1989), and the surface area of the substrate (Swindoll & Applehans, 1987). Landrum (1989) suggested that the bioavailability of sediment-sorbed chemicals declines as the contact time between the sediment and a contaminant increases. For example, Schuytema et al., (1990) observed that addition of HCB-spiked sediments did not result in a significant increase in the uptake of HCB by the worm ( Lumbriculus variegatus), amphipods ( Hyalella azteca and Gammarus lacustris), and fathead minnows ( Pimephales promelas) in a laboratory recirculating water/sediment system. However, there was a substantial increase of HCB levels in bed sediment, suggesting that sediment served as a more effective sink for HCB than the organisms. The biomagnification factor (BMF) for HCB in the earthworm Eisenia andrei after exposure via food was 0.068 on a wet weight basis (0.071 on a lipid basis) (Belfroid et al., 1994a), the biota lipid-to-soil accumulation factor, defined as the ratio of the concentration in the animal to that on the soil, was 215 g soil dry weight/g lipid (Belfroid et al., 1994b), and the bioconcentration factors (BCFs) for earthworms kept in water were found to be between 48 × 104 and 62 × 104 ml water/g lipid (Belfroid et al., 1993).
organisms at higher trophic levels, as significant biomagnification has been observed in several studies in natural aquatic ecosystems. In Lake Ontario, Oliver & Niimi (1988) observed that tissue residue concentrations increased from plankton (mean = 1.6 ng/g wet weight) to mysids (mean = 4.0 ng/g wet weight) to alewives (mean = 20 ng/g wet weight) to salmonids (mean = 38 ng/g wet weight). Braune & Norstrom (1989) used field data on body burdens of HCB in the herring gull ( Larus argentatus) and one of its principal food items, the alewife ( Alosa pseudoharengus) in a Great Lakes food chain to calculate a biomagnification factor (whole body, wet weight basis) of 31.
Representative levels reported in various environmental media in many countries are presented in Tables 4, 5 and 6.
at low concentrations. Mean concentrations of HCB in air removed from point sources in Canada, Norway, Sweden, Germany, the USA, the Arctic and the Antarctic range from 0.04 to 0.6 ng/m3 (Table 4). Levels of HCB in air are generally similar between urban, rural and remote sites, reflecting the persistence and long-range transport of this substance.
chlorinated solvent and pesticide plants in 1973 and 1976 were much higher than background levels (Spigarelli et al., 1986). Concentrations as high as 24 µg/m3 were detected in the immediate vicinity of one plant, while the maximum concentration of HCB distant from the site was 0.36 µg/m3. The highest levels were associated with the production of perchloroethylene, trichloroethylene and carbon tetrachloride, and with plants where onsite landfill and open pit waste disposal were practiced. More recently, Grimalt et al. (1994) reported that airborne concentrations of HCB in a community in the vicinity of a organochlorine factory built in 1898 in Catalonia, Spain, averaged 35 ng/m3, compared with 0.3 ng/m3 in Barcelona, the reference community for this study. It is not known how representative the data from these studies are, as HCB releases are expected to be minimized from industries using appropriate modern technology and waste management practices. No data are available on the levels of HCB in indoor air. Table 4. Levels of hexachlorobenzene in ambient air (ng/m3) Location Year Detection Mean Rangea Reference limit
Canada (Windsor, Ontario) 1987-1990 0.03 0.13 ND-0.44 Environment Canada (1992) Canada (Ontario) - industrial/urban areas 1985-1989 0.007 0.167 0.07-0.31 Lane et al. (1992b) - rural areas 0.094 0.02-0.31
(Beaufort Sea) Bear Island (Arctic) - summer
- winter 0.001 0.04 0.029-0.045 Oehme & Stray (1982) 0.001 0.111 0.059-0.188 Southern Ocean and 1990 0.06 0.04-0.078 Bidleman et al. (1993) Antarctica Enewetak Atoll 1979 0.10 0.095-0.13 Atlas & Giam (1981) (Pacific Ocean) Spitzbergen - summer 0.001 0.071 0.05-0.085 Oehme & Stray (1982) - winter 0.001 0.086 0.071-0.095
limit
Germany (Hamburg - 1986-1987 0.6 0.3-2.5 Bruckmann et al. (1988) residential, suburban and industrial sites)
- (near organochlorine 1989 & 1992 - 35 11-44 Grimalt et al. (1994) compounds factory) - hospital in Barcelona - 0.3 0.25-0.4 USA (Portland, Oregon) 1984 0.075 0.05-0.11 Ligocki et al. (1985) USA - chemical production ND-24000 Spigarelli et al. (1986) plants
a ND = not detected 5.1.2 Water Levels of HCB in freshwater in Europe and North America are generally below 1 ng/litre (Table 5), although higher values have been reported in aquatic systems that receive industrial discharges and surface run-off. In the connecting channels to the Great Lakes in Canada, HCB levels were often found to exceed 1.0 ng/litre, particularly near point sources. Levels in the St. Clair River near the Dow Chemical outfall were as high as 87 ng/litre in 1985 and 75 ng/litre in 1986 (Oliver & Kaiser, 1986). Mean concentrations of HCB in seawater rarely exceed 1 ng/litre (Table 5) (Ernst, 1986; Burton & Bennett, 1987). In the Nueces Estuary in Texas, USA, the highest level (0.61 ng/litre) was found near sewage outfalls (Ray et al., 1983a). Higher concentrations (up to 196 ng/litre) were observed in the Forth Estuary in Scotland, near domestic and chemical industry discharges (Rogers et al., 1989). 5.1.3 Soil Data identified on levels of HCB in soil are quite limited and are summarized in Table 6. The most extensive data are from the 1972 US National Soils Monitoring Program, in which the concentrations of a variety of pesticides were determined at 1483 sites from 37 states (Carey et al., 1979). HCB was detected at 11 sites, with a range of concentrations in positive samples from 10 to 440 µg/kg dry weight. Of 24 samples of agricultural soil in British Columbia, Canada, where HCB had last been applied as a seed treatment 10-15 years prior to the survey, 6 had detectable HCB residues of between 1.3 and 2.2 ng/g dry weight (Wilson & Wan, 1982). Mean concentrations of HCB reported from uncontaminated soil in Europe were found to range from 0.3 ng/g in Switzerland (Müller, 1982) to 5.1 ng/g in a Swedish rural heathland soil (Thomas et al., 1985) (it was not indicated whether concentrations were on a dry or wet weight basis). Soil from a farming area in Italy contained 40 ng/g (dry or wet weight basis not indicated) (Leoni & D'Arca, 1976). HCB levels were not markedly increased by long-term application of sludge to land in Germany at a rate of 50 to 500 tons per ha and averaged 2.8 ng/g (dry or wet weight basis not indicated) (Witte et al., 1988a,b). Monitoring programmes in Germany yielded average levels of HCB contamination of soil ranging from approximately 1 ng/g dry weight in the North Rhine-Westphalia (1990) to approximately 6 ng/g dry weight in Baden-Württemberg (1988) (BUA, 1994).
limit
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